ABSTRACT
The protective efficacy of a silkworm extract (SE) on N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism and its possible mechanisms were studied in C57BL/6 mice. Mice were administrated intraperitoneally with SE (20 mg/kg/day) for 15 days and MPTP (10 mg/kg/day) was administrated subcutaneously into the mice for the first 6 consecutive days 1 hour before SE treatment. All animals were sacrificed 24 hours after the last SE treatment. Then the parameters related to general toxicity and neurobiochemical markers, such as the dopamine level and the activities of monoamine oxidase (MAO)-B, were measured in various regions of the brain. Treatment of mice with SE effectively attenuated the MPTP-induced decline of striatal dopamine level. MAO-B activity in SE-pretreated mice was inhibited in whole brain, cerebellum and substantia nigra. These results suggest that SE plays an effective role in attenuating MPTP-induced neurotoxicity in animal model. These neuroprotective effects of SE are likely the result from the inhibitory effect on MAO-B activity in mouse brain.
Subject(s)
Animals , Mice , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine , Bombyx , Brain , Cerebellum , Dopamine , Models, Animal , Monoamine Oxidase , Neuroprotective Agents , Parkinsonian Disorders , Substantia NigraABSTRACT
The protective efficacy of a silkworm extract (SE) on N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism and its possible mechanisms were studied in C57BL/6 mice. Mice were administrated intraperitoneally with SE (20 mg/kg/day) for 15 days and MPTP (10 mg/kg/day) was administrated subcutaneously into the mice for the first 6 consecutive days 1 hour before SE treatment. All animals were sacrificed 24 hours after the last SE treatment. Then the parameters related to general toxicity and neurobiochemical markers, such as the dopamine level and the activities of monoamine oxidase (MAO)-B, were measured in various regions of the brain. Treatment of mice with SE effectively attenuated the MPTP-induced decline of striatal dopamine level. MAO-B activity in SE-pretreated mice was inhibited in whole brain, cerebellum and substantia nigra. These results suggest that SE plays an effective role in attenuating MPTP-induced neurotoxicity in animal model. These neuroprotective effects of SE are likely the result from the inhibitory effect on MAO-B activity in mouse brain.